scholarly journals An increase in galectin-3 causes cellular unresponsiveness to IFN-γ-induced signal transduction and growth inhibition in gastric cancer cells

Oncotarget ◽  
2016 ◽  
Vol 7 (12) ◽  
pp. 15150-15160 ◽  
Author(s):  
Po-Chun Tseng ◽  
Chia-Ling Chen ◽  
Yan-Shen Shan ◽  
Chiou-Feng Lin
2021 ◽  
Author(s):  
Vinayak Uppin ◽  
Shylaja M Dharmesh ◽  
Sarada R

Polysaccharides from natural sources play a significant role in the management of different cancer types including gastric cancer. In this study, we reported the effect of spirulina polysaccharide (Sp) on galectin-3 modulatory activity on gastric cancer cells. The polysaccharide was isolated from the spirulina biomass, characterized, and the in silico, in vitro studies are carried out to assess the bioactivities. The isolated Sp possessed average molecular weight of 1457 kDa, and galactose (42%) as major sugar along with Rhamnose, Arabinose, Xylose, and Mannose. Further, characterization of Sp by FT-IR and NMR spectrum indicated the presence of (β1-4D) galactose sugar with galactoarabinorhamnoglycan backbone. Among the monosaccharides, galactose showed highest binding affinity with galectin-3 protein as evidenced by the in silico interaction study. The obtained Sp, inhibited the proliferation of AGS gastric cancer cells by 48 % without affecting normal NIH/3T3 cells as opposed to doxorubicin, a known anticancer drug. Also, Sp exhibited galectin-3 mediated haemagglutination inhibition with MIC of 9.37 μg/mL compared to galactose 6.25 μg/mL, sugar specific to galectin-3. The Sp treatment significantly (p<0.05) lowered the expression of galectin-3 by 32 % compared to untreated control cells. In addition, Sp exhibited the potent cytoprotection in RBCs, Buccal cells, and DNA exposed to oxidants. Thus, the findings suggest that the polysaccharide from spirulina offer a promising therapeutic strategy in the management of gastric cancer in addition to its currently known nutritional and pharmaceutical applications.


2005 ◽  
Vol 37 (5) ◽  
pp. 391-398 ◽  
Author(s):  
Pyoung Han Hwang ◽  
Sun Young Kim ◽  
Jung Chang Lee ◽  
Sun Jun Kim ◽  
Ho Keun Yi ◽  
...  

FEBS Letters ◽  
2002 ◽  
Vol 530 (1-3) ◽  
pp. 59-64 ◽  
Author(s):  
Yasunori Kadowaki ◽  
Shunji Ishihara ◽  
Youichi Miyaoka ◽  
Mohammed Azharul Karim Rumi ◽  
Hiroshi Sato ◽  
...  

Oncotarget ◽  
2017 ◽  
Vol 8 (13) ◽  
pp. 21140-21152 ◽  
Author(s):  
Yan Li ◽  
Jianbin Ye ◽  
Zhongbiao Chen ◽  
Junjie Wen ◽  
Fei Li ◽  
...  

2021 ◽  
Vol 14 (10) ◽  
pp. 973
Author(s):  
Iwona Radziejewska ◽  
Katarzyna Supruniuk ◽  
Robert Czarnomysy ◽  
Kamila Buzun ◽  
Anna Bielawska

Afzelin demonstrates anti-inflammatory and anti-cancer properties. Our purpose was to assess its influence on apoptosis, Bax, caspases, MUC1, cancer-related carbohydrate antigens, enzymes participating in their formation, and galectin-3 in AGS gastric cancer cells. A total of 60 and 120 μM afzelin was used in all experiments. Flow cytometry was applied to determine apoptotic response. Western blotting and RT PCR were used to detect the expression of mentioned factors. Flavonoid at higher concentration revealed slight apoptotic respond. Bax, caspase-3, -8, -9 increased upon afzelin action. Stimulatory effect of the flavonoid on MUC1 cytoplasmic tail and extracellular domain in cell lysates and on MUC1 gene was revealed. MUC1 release into the culture medium was inhibited by the flavonoid. The 60 μM afzelin dose stimulated GalNAcTL5 protein expression and inhibited C1GalT1. ST6GalNAcT mRNA was inhibited by both flavonoid doses. ST3GalT was inhibited by 120 μM afzelin on protein and mRNA level. Lewisa/b protein was reduced by both afzelin concentrations. FUT3 and FUT4 mRNA was inhibited by 120 μM dose of afzelin. Galectin-3 protein increased in cell lysates and decreased in culture supernatant by 60 and 120 μM flavonoid. Galectin-3 gene expression was stimulated by two used concentrations of afzelin in comparison to control. We conclude that afzelin can be considered as the potential anti-cancer agent, supporting conventional cancer treatment.


Author(s):  
Haiyong Zhang ◽  
Jing Wu ◽  
Jinqiu Yuan ◽  
Huafu Li ◽  
Yawei Zhang ◽  
...  

Abstract Background Oxaliplatin is one of the most commonly used chemotherapeutic agent for the treatment of various cancers, including gastric cancer. It has, however, a narrow therapeutic index due to its toxicity and the occurrence of drug resistance. Hence, it is of great significance to develop novel therapies to potentiate the anti-tumor effect and reduce the toxicity of oxaliplatin. In our previous study, we demonstrated that ethaselen (BBSKE), an inhibitor of thioredoxin reductase, effectively inhibited the growth of gastric cancer cells and promoted apoptosis in vitro. In the present study, we investigated whether BBSKE can potentiate the anti-tumor effect of oxaliplatin in gastric cancer in vivo and vitro. Methods Cellular apoptosis and ROS levels were analyzed by flow cytometry. Thioredoxin reductase 1 (TrxR1) activity in gastric cancer cells, organoid and tumor tissues was determined by using the endpoint insulin reduction assay. Western blot was used to analyze the expressions of the indicated proteins. Nude mice xenograft models were used to test the effects of BBSKE and oxaliplatin combinations on gastric cancer cell growth in vivo. In addition, we also used the combined treatment of BBSKE and oxaliplatin in three cases of gastric cancer Patient-Derived organoid (GC-PDO) to detect the anti-tumor effect. Results We found that BBSKE significantly enhanced oxaliplatin-induced growth inhibition in gastric cancer cells by inhibiting TrxR1 activity. Because of the inhibition of TrxR1 activity, BBSKE synergized with oxaliplatin to enhance the production of ROS and activate p38 and JNK signaling pathways which eventually induced apoptosis of gastric cancer cells. In vivo, we also found that BBSKE synergized with oxaliplatin to suppress the gastric cancer tumor growth in xenograft nude mice model, accompanied by the reduced TrxR1 activity. Remarkably, we found that BBSKE attenuated body weight loss evoked by oxaliplatin treatment. We also used three cases of GC-PDO and found that the combined treatment of BBSKE and oxaliplatin dramatically inhibited the growth and viability of GC-PDO with increased ROS level, decreased TrxR1 activity and enhanced apoptosis. Conclusions This study elucidates the underlying mechanisms of synergistic effect of BBSKE and oxaliplatin, and suggests that the combined treatment has potential value in gastric cancer therapy.


Sign in / Sign up

Export Citation Format

Share Document